Institution
Princess Anne Hospital
Healthcare•Southampton, United Kingdom•
About: Princess Anne Hospital is a healthcare organization based out in Southampton, United Kingdom. It is known for research contribution in the topics: Population & Breast cancer. The organization has 423 authors who have published 709 publications receiving 44790 citations.
Topics: Population, Breast cancer, Cancer, Pregnancy, Germline mutation
Papers published on a yearly basis
Papers
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TL;DR: Enhanced recovery pathways improve the quality and experience of care for patients undergoing elective gynaecology surgery and enable patients to recover more quickly and leave hospital sooner.
Abstract: Key content
Enhanced recovery pathways improve the quality and experience of care for patients undergoing elective gynaecology surgery.
Enhanced recovery pathways enable patients to recover more quickly and leave hospital sooner.
Enhanced recovery pathways reduce physical and psychological stress on patients.
Enhanced recovery pathways involve patients in their own care, which leads to better outcomes.
Learning objectives
To understand the principles and benefits of enhanced recovery pathways.
To share learning and experience of enhanced recovery pathways.
Ethical issues
Further research in the form of a randomised controlled trial of enhanced recovery versus ‘old fashioned’ care would be difficult as denying aspects of care would not be ethical.
17 citations
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TL;DR: Inverted Duplication of 1q32.1 to 1q44 Characterized by Array CGH and Review of Distal 1q Partial Trisomy Meena Balasubramanian are Characterized.
Abstract: Inverted Duplication of 1q32.1 to 1q44 Characterized by Array CGH and Review of Distal 1q Partial Trisomy Meena Balasubramanian,* John C.K. Barber, Morag N. Collinson, Shuwen Huang, Viv K. Maloney, Dave Bunyan, and Nicki Foulds Wessex Clinical Genetics Service, Southampton University Hospitals Trust, Princess Anne Hospital, Southampton, UK Wessex Regional Genetics Laboratory, Salisbury NHS Foundation Trust, Salisbury District Hospital, Salisbury, UK National Genetics Reference Laboratory (Wessex), Salisbury NHS Foundation Trust, Salisbury District Hospital, Salisbury, UK Human Genetics Division, Southampton University Hospitals Trust, Southampton, UK
17 citations
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TL;DR: A study visit of six selected North American neonatal units and NNP training programmes was undertaken by a group consisting of one paediatrician and four senior neonatal nurses to evaluate the clinical role of NNPs working in neonatal intensive care units.
Abstract: Although the professional role of neonatal nurse practitioners (NNPs) has been fully integrated into many neonatal units outside the UK over the past decade,' 2 there has to date been no such development in this country. Indeed, there have been serious reservations among members of the neonatal nursing profession concerning the introduction of NNPs given the current structure and funding of neonatal care in the UK.3 Despite these reservations, it has for several years been the view of most of the paediatricians and of many neonatal nurses within the Wessex region that the care of sick newborn infants could be improved by extending the role of the neonatal nurse. The case for extending the role has now been accepted by medical and nurse managers within the region and plans are well advanced to establish an educational course in Southampton for the development of NNPs in Wessex. In planning this radical innovation it was felt that much could be learnt, and many problems possibly avoided, by examining the training and professional role of NNPs in North America. A study visit of six selected North American neonatal units and NNP training programmes was, therefore, undertaken by a group consisting of one paediatrician and four senior neonatal nurses. The two main aims of the visit were: (i) to study the NNP training programmes and (ii) to evaluate the clinical role of NNPs working in neonatal intensive care units.
17 citations
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TL;DR: The aim of this paper is to study the safety and efficacy of once daily gentamicin in neonates ≥32 weeks of gestation and ≤7 days of age.
Abstract: Aim: The aim of this paper is to study the safety and efficacy (measured by therapeutic level) of once daily gentamicin in neonates ≥32 weeks of gestation and ≤7 days of age.
Setting: Level II neonatal intensive care unit.
Subjects: Neonates ≥32 weeks of gestation and ≤7 days of age treated with gentamicin for presumed sepsis.
Methods: Gentamicin was administered by intravenous injection at 4 mg/kg/day once daily. Peak and trough gentamicin levels were measured at the third dose.
Results: In neonates with gestational age between 32 and 36 weeks, 14 out of 65 (22%) had trough serum concentration >2 mg/L. Only 39 (60%) had peak and trough levels within the therapeutic range. All babies who had audiometric evaluation (62 out of 65) had normal hearing. Out of the 65 babies, 60 had paired serum creatinine levels estimated and none had evidence of renal dysfunction. Among term neonates, only 2 out of 50 had the trough serum concentration of >2 mg/L. In 38 (76%) of the 50 neonates, the trough serum gentamicin concentration was <2.0 mg/L and the peak level was <10 mg/L. Forty-eight babies had audiometric evaluation which was normal.
Conclusion: A dose of 4 mg/kg/day produces serum gentamicin levels outside the therapeutic range in two-fifths of neonates between 32 and 36 ± 6 weeks. A single dose of 4 mg/kg/day of gentamicin is appropriate for term babies and probably excessive for 32–36 weeks’ neonates.
17 citations
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TL;DR: In this paper, a family and fetus with two SHOX mutations were described, and the fetus inherited an additional Xp deletion (Xpter-Xp22.12) that also included the SHOX gene from her chromosomally normal father.
Abstract: Leri-Weill dyschondrosteosis (LWD) and Langer mesomelic dysplasia (LMD) are caused by mutations in the SHOX gene. LWD results from haploinsufficiency and is dominantly inherited, while the more severe LMD results from the homozygous loss of SHOX. We describe a family and fetus with two SHOX mutations. Several relatives carry an approximately 200 kb interstitial deletion that includes the whole SHOX gene. Their condition is mild, with no Madelung deformity, and was originally diagnosed as hypochondroplasia (HCH). This deletion was also transmitted to a female fetus. However, unlike her carrier relatives, the ultrasound scan of the fetus and subsequent autopsy were consistent with LMD. The fetus inherited an additional Xp deletion (Xpter-Xp22.12) that also included the SHOX gene from her chromosomally normal father. This represents a unique molecular condition for LMD: the fetus is a compound heterozygote with two independent deletions, one inherited and one arising from a de novo event.
17 citations
Authors
Showing all 423 results
Name | H-index | Papers | Citations |
---|---|---|---|
Richard S. Houlston | 110 | 768 | 50101 |
Andrew Collins | 100 | 684 | 40634 |
Alan Jackson | 99 | 743 | 42969 |
Declan G. Murphy | 95 | 820 | 37076 |
Mark A. Hanson | 93 | 545 | 38985 |
Diana Eccles | 90 | 354 | 36226 |
Ian G. Campbell | 71 | 303 | 18596 |
Nick S. Macklon | 68 | 261 | 15593 |
Stuart L. Stanton | 63 | 201 | 13464 |
Amit Sharma | 61 | 551 | 13597 |
Judith Rankin | 57 | 273 | 11193 |
Pietro Liò | 54 | 613 | 20137 |
Denis C. Shields | 54 | 223 | 12677 |
Abdul H. Sultan | 53 | 219 | 11528 |
Anneke Lucassen | 51 | 193 | 9851 |